Using fundamental knowledge of induced resistance to develop control strategies for bacterial canker of kiwifruit caused by Pseudomonas syringae pv. actinidiae

Pseudomonas syringae pv. actinidiae (Psa) which causes bacterial canker of kiwifruit (Actinidia deliciosa and A. chinensis) was first isolated in Japan in 1984 (Takikawa et al., 1989), and soon after in Korea (Koh et al., 1994) and Italy (Scortichini, 1994). The economic impact on the global production of kiwifruit of those early occurrences was relatively limited (Vanneste et al., 2011). However, the latest outbreak of Psa which started in Italy in 2008 and rapidly spread throughout most of the kiwifruit growing regions of the world, represents a major threat to the global kiwifruit industry (Vanneste, 2012). The pathovar actinidiae is not a genetically homogeneous pathovar; strains can be grouped in four biovars based on their molecular, microbiological and pathogenic characteristics (Vanneste et al., 2013) which is consistent with MLST and whole genome sequence analysis (Ferrante and Scortichini, 2010; Mazzaglia et al., 2011; Chapman et al., 2012). The recent outbreak of bacterial canker on kiwifruit in Europe and New Zealand is caused by the same biovar of Psa (biovar 3) (Chapman et al., 2012; Vanneste et al., 2013). During the 2 years that the pathogen has been present in New Zealand, over 60% of the area planted in kiwifruit has been affected (Kiwifruit Vine Health, 2012). This rapid spread may be attributable to the virulence of biovar 3 and to the scarcity of products available for control of plant pathogenic bacteria in general, and Psa in particular. Many products used for control of plant pathogenic bacteria contain antibiotics (mostly streptomycin) or heavy metals (mostly copper). Both types of products do have limitations because of phytotoxicity or because they are not authorized in some countries (e.g., antibiotics in Europe). This has led to a large screening programme in New Zealand for the identification of potentially effective products to control Psa. The products tested included a number of commercially available potential elicitors of host resistance. One of the most effective elicitors in glasshouse trials on A. chinensis and A. deliciosa was acibenzolar-S-methyl [ASM], sold under the names of Bion® or Actigard® (Syngenta). ASM belongs to the benzothiadiazole chemical group and operates as a functional analogue of salicylic acid. It has demonstrated good efficacy against bacterial diseases, including bacterial spot (Xanthomonas axonopodis pv. vesicatoria) and bacterial speck (P. syringae pv. tomato) in tomato (Louws et al., 2001), fire blight (Erwinia amylovora) in apples (Bastas and Maden, 2007), pear (Spinelli et al., 2006) and quince (Bastas and Maden, 2007), and xanthomonas leaf blight (X. axonopodis pv. allii) in onions (Gent and Schwartz, 2005). However, while elicitors can be very effective in controlled conditions, the host response can be highly variable in the field, thus raising questions about their potential for disease management. Furthermore, there is evidence that induced resistance, whether via the use of chemical elicitors or by constitutive expression of inducible defenses, can be accompanied by reduced fruit production and/or quality (Walters and Heil, 2007; Cipollini and Heil, 2010). These observations are consistent with the theory that induced resistance evolved as a strategy to minimize the metabolic costs associated with defense (Karban, 2011). Plant genotype and environment factors can also affect the relative benefits and costs of induced resistance (Cipollini and Heil, 2010; Walters et al., 2011) and a greater understanding of these dynamic interactions is necessary to facilitate more effective use of elicitors for disease control. Complementary studies that target both fundamental and applied aspects of plant innate immunity are critical to realize the potential of induced resistance. Typically, inducible defenses are triggered upon recognition of pathogenderived molecules. These molecules were historically termed elicitors or avirulence factors, but have more recently been renamed microbe-associated molecular patterns (MAMPs) and effectors, respectively (Jones and Dangl, 2006; Bent and Mackey, 2007). Phytohormone-mediated signaling pathways play a key role in orchestrating the plant response, with cross-talk between salicylic acid (SA), jasmonic acid (JA), and ethylene (ET) pathways providing means whereby the plant can tailor its defense response to different pathogens and pests (Robert-Seilaniantz et al., 2011; Pieterse et al., 2012). The SA and JA/ET defense pathways are often mutually antagonistic. However, synergistic interactions have been reported in some pathosystems (Pieterse et al., 2009). Abscisic acid (ABA) has also been shown to interact with defense-signaling pathways and it is proposed that ABA operates as a global regulator and co-ordinates the plant response to simultaneous multiple stresses (Ton et al., 2009). ABA-regulated